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Managing STEMI Mimics in the Prehospital Environment

Managing STEMI Mimics in the Prehospital Environment

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Managing STEMI Mimics in the Prehospital Environment

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  1. Managing STEMI Mimics in the Prehospital Environment Brandon Oto, NREMT-B

  2. The Problem: Most STE is not MI … and most providers can’t tell the difference

  3. “Unfortunately, STE is a not an uncommon finding on the ECG of the chest pain patient; its cause infrequently involves AMI.” Brady et al., Electrocardiographic ST-segment elevation: correct identification of acute myocardial infarction (AMI) and non-AMI syndromes by emergency physicians (Acad Emerg Med 2001; 8(4):349-360)

  4. How common? Brady et al., Cause of ST segment abnormality in ED chest pain patients (Am J Emerg Med 2001 Jan;19(1):25-8) • Retrospective review of ED charts over 3-month period • Looked at 902 adults with cc “chest pain” • Looked for STE in contiguous leads, >1mm limb leads, >2mm precordials • Compared final diagnoses, MI vs. other

  5. Results Only 15% of STE patients had MI! 85% had non-MI diagnosis

  6. What were they? • Left Ventricular Hypertrophy — 25% • Left Bundle Branch Block — 15% • AMI — 15% • Benign Early Repolarization — 12% • Right Bundle Branch Block — 5% • Nonspecific BBB — 5% • Ventricular aneurysm — 3% • Pericarditis — 1% • Undefined/unknown — 17% STEMI-mimic was 6 times as likely as STEMI! MI was not even single most likely cause!

  7. In other words: Any monkey can recognize ST elevation STEMI recognition and diagnosis requires distinguishing MI from non- ischemic causes

  8. How do we do at this? Bad! 51% false-positive rate Sejersten et al. Comparison of the Ability of Paramedics With That of Cardiologists in Diagnosing ST-Segment Elevation Acute Myocardial Infarction in Patients With Acute Chest Pain (Am J Cardiol 2002 Nov 1;90(9):995-8) Half of our diagnoses were wrong

  9. Why does it matter? Maybe it doesn’t! Overtriage is better than undertriage… Maybe it’s better to play it safe… But there are downsides

  10. Downsides of false positive STEMI diagnoses • Compromises systems. Cath labs that can’t rely on you eventually won’t activate for you. Increased D2B times. • Weakens true positives. If you lack confidence in recognizing mimics, you’ll lack confidence in making the call for true STEMI. • Degrades professional respect. Field providers that do their job right encourage further development of progressive EMS-hospital interfaces.

  11. More downsides of false positive STEMI diagnoses • Missed alternate diagnoses. Some non-MI diagnoses are also critical – think aortic dissection, hyperkalemia, etc. “Call it STEMI” is not always “playing it safe.” • Wrong treatment. Nitro? Aspirin? Fibrinolytics? Getting it right affects field and hospital treatment. • Wrong transport destination. Unnecessarily bypassing non-PCI hospitals damages continuity of care, burdens families, antagonizes facilities.

  12. More downsides of false positive STEMI diagnoses • Stretches limited resources and causes iatrogenic harm. • Inappropriate activation from the field will not always be reversed by ED/cardiology upon arrival due to liability • Unnecessary activations tax staff and facilities, divert resources from other patients • Unnecessary angiography (or worse, thrombolysis) can cause renal/vascular damage • Wrongly rushing the patient to the cath lab means they aren’t getting treated for their real problems

  13. More downsides of false positive STEMI diagnoses “… the issue of false-positive catheterization laboratory activation remains a significant concern because unnecessary emergency coronary angiography is not without risk to the patient and may impose a burden on limited human and physical catheterization laboratory resources.” Larson et al, "False-Positive" Cardiac Catheterization Laboratory Activation Among Patients With Suspected ST-Segment Elevation Myocardial Infarction. JAMA. 2007;298(23):2754-2760.

  14. What are our tools for addressing this? • Clinical correlation. Any suspicious ECG findings should be matched against patient presentation and physical exam. • History and risk factors. Does hx supports MI – smoker, diabetic, hypertensive, aspirin use, etc? • Old ECGs. Extremely valuable tool when available for establishing baseline. • Serial ECGs. Repeat 12-leads may reveal dynamic changes with time/treatment.

  15. More tools for addressing this • Supportive ECG findings. Subtler red flags (pink flags?) that further support or undermine diagnosis of STEMI. • Expert consultation. Upload or interface with medical control, where available. • Computer interpretation. Automatic algorithms provide a “virtual consult,” an always-available second opinion.

  16. More tools for addressing this But wait! • No clinical sign/symptoms are completely reliable • No ECG findings are completely reliable • Hx regularly fools us The answer? You must look at the whole picture Diagnosis is based on a constellation of datapoints – not any one finding!

  17. Computer interpretations Useless? Infallible? Neither! Just another tool. Understanding its strengths and weaknesses is essential to effective use

  18. GE Marquette 12SL Developed in 1980, continuously updated since Used in most cardiac monitors including Zoll, Lifepack, most in-hospital monitors – but not the Philips MRx *** ACUTE MI SUSPECTED *** ~100% specific! ~61% sensitive Massel D et al., Strict reliance on a computer algorithm or measurable ST segment criteria may lead to errors in thrombolytic therapy eligibility. Am Heart J 2000 Aug; 140(2) 2216

  19. GE Marquette 12SL Bottom line: *** ACUTE MI SUSPECTED *** Not very sensitive But very specific Exactly what we need! Great tool for screening out false positives

  20. GE Marquette 12SL Caveats: • Very dependent on data quality! • Stable baseline • No artifact • Proper electrode placement • Zoll may warn you: “Poor data quality, interpretation may be adversely affected” • Fooled by SVT – distrust interpretations with HR > 100 • Can be fooled by PR depression

  21. GE Marquette 12SL More on data quality: • Proper precordial placement • Limb electrodes go on the limbs • Manage shivering • Park the truck if necessary • Prevent patient movement • May need to prepare skin – shave, dry, tincture? • Undress fully from waist up when appropriate • Stay organized

  22. Signs that point to MI Your basic model for STEMI should be: Significant ST elevation in contiguous leads, with reciprocal changes, in the setting of clinical correlation • Significant means significant relative to the QRS amplitude; microvoltages = small STE! • Contiguous means: know your coronary arteries to understand which occlusions make anatomical sense (“go together”)

  23. Signs that point to MI Your basic model for STEMI should be: Significant ST elevation in contiguous leads, with reciprocal changes, in the setting of clinical correlation • Reciprocal changes are the most valuable addition to your basic criteria for increased specificity (90+%). Look closely; changes may be subtle. Akhras, et al. Reciprocal change in ST segment in acute myocardial infarction: correlation with findings on exercise electrocardiography and coronary angiography. Br Med J (Clin Res Ed). 1985 June 29; 290(6486): 1931–1934. Otto, et al. Evaluation of ST segment elevation criteria for the prehospital electrocardiographic diagnosis for acute myocardial infarction. Ann Emerg Med. 1994 Jan;23(1):17-24.

  24. Signs that point to MI Your basic model for STEMI should be: Significant ST elevation in contiguous leads, with reciprocal changes, in the setting of clinical correlation • Reciprocal changes may also be your only indication of posterior-wall MI. Have a high index of suspicion and consider V7–V9. A riddle: why does every patient seem to breathe 16 times a minute?

  25. Signs that point to MI Your basic model for STEMI should be: Significant ST elevation in contiguous leads, with reciprocal changes, in the setting of clinical correlation • Clinical correlation means the classics (CP, dyspnea, N/V, etc.) but also everything from dandruff to microdeckia. Be open! • 1/4 – 1/3 may present with unusual or no complaints. Elderly, diabetics, females, cardiac hx more likely to present atypically, and have worse prognosis. Pope et al. Missed Diagnoses of Acute Cardiac Ischemia in the Emergency Department. N Engl J Med 2000; 342:1163-1170 Kannel. Silent myocardial ischemia and infarction: insights from the Framingham Study. Cardiol Clin. 1986 Nov;4(4):583-91.

  26. More signs that point to MI • ST morphology. Most benign elevation presents with concave (scooped) ST segments; convex (rounded) elevation is a fairly specific indicator of MI. • For ST depression, flip it over, same thing • 97% specific; 77% sensitive Brady et al. Electrocardiographic ST-segment elevation: the diagnosis of acute myocardial infarction by morphologic analysis of the ST segment. Acad Emerg Med. 2001 Oct;8(10):961-7.

  27. More signs that point to MI • Changes on serial ECGs. ACS is a dynamic process of supply/demand imbalance; consecutive 12-leads should reveal ongoing changes. Mimics are typically electrically stable. • When possible, obtain an initial ECG prior to treatment; oxygen/nitro may erase ischemic changes. • Perform serial recordings and watch for evolution over time; subtle becomes obvious, NSTEMI becomes STEMI, etc. Any changes are suspicious. • One of the best tools for distinguishing STEMI vs. mimics! Early and continuous prehospital ECGs can play a crucial role in eventual care!

  28. More signs that point to MI • Changes from old ECGs. When available (from facility or patient), previous 12-leads can establish a baseline -- but this only proves changes since the time of that tracing.

  29. Sgarbossa’s Criteria Aka The rule of appropriate discordance Aka The gift that keeps on giving Originally developed in 1996 as system for ruling in MI in setting of LBBB Sgarbossa et al. Electrocardiographic Diagnosis of Evolving Acute Myocardial Infarction in the Presence of Left Bundle-Branch Block. N Engl J Med 1996; 334:481-487February 22, 1996

  30. Sgarbossa’s Criteria The rule of appropriate discordance: • A QRS with a positive terminal deflection should be followed by a negatively shifted ST/T (ST depression, T wave inversion) • A QRS with a negative terminal deflection should be followed by a positively deflected ST/T (ST elevation, upright T wave) • ST elevation/depression should be proportional to the size of the QRS

  31. Sgarbossa’s Criteria Deviations from this suggest MI!

  32. Sgarbossa’s Criteria This principle applies to: • LBBB • RBBB • LVH (“strain pattern”) • Paced ventricular rhythms • Non-paced ventricular rhythms (including PVCs) • WPW and other preexcitation How useful!

  33. Sgarbossa’s Criteria The actual criteria In the setting of chest pain and LBBB: • Concordant STE ≥1mm in any lead with a positive QRS (5 points) • Concordant ST depression ≥1mm in V1, V2, or V3 (3 points) • Discordant ST elevation ≥5mm in any lead with negative QRS Sum up the points: ≥3 is 98% specific for MI, 20% sensitive ≥2 is 61–100% specific, 20–79% sensitive Tabas et al. Electrocardiographic criteria for detecting acute myocardial infarction in patients with left bundle branch block: a meta-analysis. Ann Emerg Med. 2008 Oct;52(4):329-336.e1. Epub 2008 Mar 17.

  34. Sgarbossa’s Criteria “Discordant ST elevation ≥5mm in any lead with negative QRS” • The most controversial rule due to the lowest specificity • The majority of problems arise with large amplitudes (LVH), when 5mm may be normal discordance

  35. Sgarbossa’s Criteria Smith’s Modification Make it proportional! “Discordant ST elevation ≥.2 (1/5) of terminal S wave” • Reduces false positives from large QRS • May reduce false negatives from small QRS (microvoltages) Smith et al. (2012) Diagnosis of ST-Elevation Myocardial Infarction in the Presence of Left Bundle Branch Block With the ST-Elevation to S-Wave Ratio in a Modified Sgarbossa Rule. Ann Emerg Med. 2012 Aug 31 Epub

  36. Sgarbossa’s Criteria Modified or not, has the sensitivity/specificity of Sgarbossa been studied for any rhythm except LBBB? Paced ventricular rhythms (similar results) … and nothing else! Does it work for LVH, etc? Yes! Use the principles – don’t sweat the numbers

  37. Now, bring in the mimics!

  38. Left Ventricular Hypertrophy • Single most common STEMI mimic • May or may not exhibit ST changes • Sgarbossa works well when it does • Can be difficult to determine true size of QRS (overprinting or clipping) • Tip: True anterior STEMI almost never present in setting of profound LVH • Tip: ST segment may be benignly convex • Voltage criteria generally irrelevant to question of MI Dr. Smith, unpublished

  39. Left Bundle Branch Block A big can of worms. • Second most common STEMI mimic • Traditionally either considered “nondiagnostic,” or de facto evidence of MI. AHA still recommends fibrinolysis/TPA: “… in patients with [signs/symptoms of ACS and] … new or presumably new left bundle branch block …” Why? “… because they have the highest mortality rate when LBBB is due to extensive AMI” 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Part 10: Acute Coronary Syndromes

  40. Left Bundle Branch Block (The pathophysiology here probably stems from the fact that a LAD occlusion proximal enough to involve the bundle branches is endangering a great deal of myocardium.) Another, implicit reason is because MI is difficult to definitively diagnose in the setting of LBBB. Prehospitally, the result is that new LBBB is often assumed to be AMI.

  41. Left Bundle Branch Block Problem #1: How do you know it’s “new”? Answer: Patient history Answer: Old ECGs Answer: You can’t

  42. Left Bundle Branch Block Problem #2: Even “new” LBBB is not an indicator of MI! 2008 observational study looked at three groups of ED patients with complaints of ACS: • Those with new LBBB • Those with old LBBB • Those with no LBBB Result: All groups had equal probability of AMI Chang et al. Lack of association between left bundle-branch block and acute myocardial infarction in symptomatic ED patients. American Journal of Emergency Medicine (2009) 27, 916–921

  43. Left Bundle Branch Block In short: new LBBB in the setting of AMI may be an indicator of high risk But it is not an indicator of AMI! Diagnosis must still occur.